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Journal of Virology, January 2007, p. 95-105, Vol. 81, No. 1
0022-538X/07/$08.00+0     doi:10.1128/JVI.01608-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Adenovirus Type 5 Early Region 1B 156R Protein Promotes Cell Transformation Independently of Repression of p53-Stimulated Transcription{triangledown}

Timo Sieber1 and Thomas Dobner2*

Institut für Medizinische Mikrobiologie und Hygiene, Universität Regensburg, Landshuter Strasse 22, D-93047 Regensburg, Germany,1 Heinrich Pette Institute for Experimental Virology and Immunology, Department of Molecular Virology, Martinistrasse 52, D-20251 Hamburg, Germany2

Received 27 July 2006/ Accepted 8 October 2006

Early region 1B (E1B) of adenovirus type 5 (Ad5) encodes at least five different polypeptides generated by alternative splicing of a common mRNA precursor. Two of these gene products, E1B-19K and E1B-55K, are individually capable of cooperating with the Ad5 E1A proteins to completely transform rodent cells in culture. Substantial evidence suggests that these two E1B proteins contribute to cell transformation by antagonizing growth arrest and apoptosis. Here, we performed genetic and biochemical analyses to assess the attributes of the remaining E1B proteins (E1B-156R, E1B-93R, and E1B-84R). Our results show that E1B-156R, which comprises the 79 amino-terminal and 77 carboxy-terminal amino acids of E1B-55K, also enhances focal transformation of primary rat cells in cooperation with E1A. Since E1B-156R seemed unable to relocalize p53 and inhibit its transactivating function, it must be assumed that it contributes to transformation independently of repression of p53-stimulated transcription. Furthermore, we discovered that E1B-156R contains a functional transcriptional repression domain and binds Ad5 E4orf6 and the cellular apoptosis regulator Daxx. While the ability to bind E4orf6 could indicate further biological functions of E1B-156R in viral infection, the interaction with Daxx might also be linked to its transforming potential. Taken together, these analyses introduce E1B-156R as a novel transformation-promoting E1B protein that acts without repressing p53 transactivation. Moreover, identification of the interaction partners E4orf6 and Daxx provides a first glance of E1B-156R's potential functions.

* Corresponding author. Mailing address: Heinrich Pette Institute for Experimental Virology and Immunology, Dept. of Molecular Virology, Martinistrasse 52, D-20251 Hamburg, Germany. Phone: 49 40 48051 287. Fax: 49 40 48051 103. E-mail: thomas.dobner{at}hpi.uni-hamburg.de.

{triangledown} Published ahead of print on 18 October 2006.

Journal of Virology, January 2007, p. 95-105, Vol. 81, No. 1
0022-538X/07/$08.00+0     doi:10.1128/JVI.01608-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.



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